title: Sodium hydrosulfide prevents hypoxia-induced behavioral impairment in neonatal mice.
abstract: Hypoxic encephalopathy is a common cause of neonatal seizures and long-term neurological abnormalities. Endogenous hydrogen sulfide (H2S) may have multiple functions in brain. The aim of this study is to investigate whether sodium hydrosulfide (NaHS), a H2S donor, provides protection against neonatal hypoxia-induced neurobehavioral deficits. Neonatal mice were subjected to hypoxia (5% oxygen for 120min) at postnatal day 1 and received NaHS (5.6mg/kg) once daily for 3d. Neurobehavioral toxicity was examined at 3-30d after hypoxia. Treatment with NaHS significantly attenuated the delayed development of sensory and motor reflexes induced by hypoxia up to two weeks after the insult. Moreover, NaHS improved the learning and memory performance of hypoxic animals as indicated in Morris water maze test at 30d after hypoxia. In mice exposed to hypoxia, treatment with NaHS enhanced expression of brain derived neurotrophic factor (BDNF) in the hippocampus. Furthermore, the protective effects of NaHS were associated with its ability to repress the hypoxia-induced nitric oxide synthase (NOS) activity and nitric oxide production in the hippocampus of mice brain. Taken together, these results suggest that the long-lasting beneficial effects of NaHS on hypoxia-induced neurobehavioral deficits are mediated, at least in part, by inducing BDNF expression and suppressing NOS activity in the brain of mice.
authors.affiliation: Institution of Physiology, Shandong University School of Medicine, 44# Wenhua Xi Road, Jinan, Shandong 250012, PR China.
authors.forename: Zhen
authors.initials: Z
authors.lastname: Wang
authors.forename: Jingmin
authors.initials: J
authors.lastname: Zhan
authors.forename: Xueer
authors.initials: X
authors.lastname: Wang
authors.forename: Jianhua
authors.initials: J
authors.lastname: Gu
authors.forename: Kai
authors.initials: K
authors.lastname: Xie
authors.forename: Qingrui
authors.initials: Q
authors.lastname: Zhang
authors.forename: Dexiang
authors.initials: D
authors.lastname: Liu
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001522:Behavior, Animal; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism; D005260:Female; D006624:Hippocampus / Q000378:metabolism; D002534:Hypoxia, Brain / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D018782:Maze Learning / Q000502:physiology; D008569:Memory Disorders / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D051379:Mice; D008807:Mice, Inbred BALB C; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism; D013440:Sulfides / Q000627:therapeutic use*
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D013440:Sulfides; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; C025451:sodium bisulfide
keywords: Brain derived neurotrophic factor; Hypoxia; Nitric oxide; Sodium hydrosulfide